摘要
目的初步探讨血浆6-酮-前列腺素F1α(6-酮-PGF1α)、8-表氧-前列腺素F2α(8-表氧-PGF2α)和11-去氢-血栓烷B2(DH-TXB2)水平在狼疮肾炎(LN)中的临床意义。方法采用酶联免疫吸附试验(ELISA)和放射免疫法对46例LN患者和20名正常对照进行血浆6-酮-PGF1α、8-表氧-PGF2α和DH-TXB2等检测,分别分析其与系统性红斑狼疮活动指数(SLEDAI)、血清抗dsDNA抗体、补体C3、24h尿蛋白定量及内生肌酐清除率(Ccr)的相关关系,同时观察治疗后上述指标的变化。结果①LN组患者血浆6-酮-PGF1α水平显著低于对照组(P<0.05),且活动期组显著低于非活动期组(P<0.05),而LN组患者血浆8-表氧-PGF2α、DH-TXB2均显著高于对照组,且活动期组均显著高于非活动期组。②经相关分析,血浆6-酮-PGF1α水平与SLEDAI、血清抗dsDNA抗体呈负相关,与C3呈正相关;血浆8-表氧-PGF2α及DH-TXB2均与SLEDAI、血清抗dsDNA抗体呈正相关,与C3、Ccr呈负相关。经综合治疗后,血浆6-酮-PGF1α显著升高,8-表氧-PGF2α及DH-TXB2均显著降低。结论血管内皮损伤、脂质过氧化及血小板活化是LN的发生、发展的重要机制。
Objective To investigate the clinical significance of plasma 6-keto-prostaglandin F1α (6-keto-PGF1α)、 8-epi-prostaglandin F2α (8-epi-PGF2α) and 11-dehydrothromboxane B2 (DH-TXB2) in patients with lupus nephritis (LN). Methods ELISA assay and radioimmunoassay were applied to evaluate the plasma 6-keto-PGF1α、 8-epi-PGF2α and DH-TXB2 levels in 46 LN patients and 20 normal controls. The relationship of these indices with the SLE disease activity index (SLEDAI)、 anti-dsDNA、 C3、 24 hour urine protein、 endogenous creatinine clearance rate (Ccr) was analysed. Restults {1} Plasma 6-keto-PGF1α level of LN was lower than that of normal control group, while it was lower in active SLE than that of the quiescent. The results also showed the concentrations of pasma 8-epi-prostaglandin F2α and DH-TXB2 in LN patients were significantly increased than those of normal controls. {2} The parametes in active SLE patients were significantly higher than those in quiescent patients. The concentration of 6-keto-PGF1α was negtively correlated with SLEDAI, anti-dsDNA, but positively correlated with C3 and no relationship was observed with 24 hour urine protein, while the levels of 8-epi-PGF2α and DH-TXB2 were postively correlated with SLEDAI、 anti-dsDNA, negatively correlated with C3, Ccr, respectively, but no relationship with 24 hour urine protein. The level of 8-epi-PGF2α and DH-TXB2 in 28 LN patients was significantly reduced and 6-keto-PGF1α was significantly increased after therapy. Conclusion The injury of endothelial cell, oxidative stress and platelet activation may be one of the mechanisms of LN progress.
出处
《中华风湿病学杂志》
CAS
CSCD
2004年第10期614-617,共4页
Chinese Journal of Rheumatology